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      Salt Sensitivity of Blood Pressure in Humans

      Author(s): 1
      Publication date Created:
      Publication date (Print):
      Journal: Hypertension
      Publisher: Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          A variety of different techniques have been used for the assessment of the blood pressure response to changes in salt and water balance in humans. These have generally been found to be reproducible and to yield congruent results. This review surveys the characteristics of subjects identified as salt sensitive and salt resistant by different investigators from demographic and physiological perspectives.

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          A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension.

          Robert Dluhy, Ann Powers, R Lifton … (1992)
          Glucocorticoid-remediable aldosteronism (GRA), an autosomal dominant disorder, is characterized by hypertension with variable hyperaldosteronism and by high levels of the abnormal adrenal steroids 18-oxocortisol and 18-hydroxycortisol, which are all under control of adrenocorticotropic hormone and suppressible by glucocorticoids. These abnormalities could result from ectopic expression of aldosterone synthase, which is normally expressed only in adrenal glomerulosa, in the adrenal fasciculata. Genes encoding aldosterone synthase and steroid 11 beta-hydroxylase (expressed in both adrenal fasciculata and glomerulosa), which are 95% identical and lie on chromosome 8q (refs 7, 10), are therefore candidate genes for GRA. Here we demonstrate complete linkage of GRA in a large kindred to a gene duplication arising from unequal crossing over, fusing the 5' regulatory region of 11 beta-hydroxylase to the coding sequences of aldosterone synthase (maximum lod score 5.23 for complete linkage, odds ratio of 170,000:1). This mutation can account for all the physiological abnormalities of GRA. Our result represents the demonstration of a mutation causing hypertension in otherwise phenotypically normal animals or humans.
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            The effect of high-sodium and low-sodium intakes on blood pressure and other related variables in human subjects with idiopathic hypertension.

            B Kawasaki, Lois E. H. Smith, C S Delea … (1978)
            Nineteen patients with hypertension in whom all known causes of blood pressure elevation had been ruled out were classified as "salt-sensitive" or "nonsalt-sensitive" from the changes in blood pressure with changes in sodium intake from 9 meq to 249 meq/day. With the diet containing 249 meq sodium per day, there were no statistically significant differences in plasma sodium, potassium, chloride, aldosterone, cortisol or renin activity, or in urinary potassium, aldosterone or 17-hydroxycorticosteroids between the two groups. The "salt-sensitive" patients retained more sodium on the high-sodium diet than did the patients who were not sensitive to salt ("nonsalt-sensitive"); accordingly, sodium induced more weight gain in the salt-sensitive patients.
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              The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents.

              V Katch, R Matthew Chico, D Bondie … (1989)
              To clarify the role of sodium intake in the regulation of blood pressure in obese subjects, we measured blood pressure in 60 obese and 18 nonobese adolescents after successive two-week periods of a high-salt diet (greater than 250 mmol of sodium per day) and a low-salt diet (less than 30 mmol per day). When they were changed from a high-salt to a low-salt diet, the obese group had a significantly larger mean change (+/- SE) in mean arterial pressure (-12 +/- 1 mm Hg) than did the nonobese group (+1 +/- 2 mm Hg; P less than 0.001). The variables that best predicted the degree of sodium sensitivity were the fasting plasma insulin level, the plasma aldosterone level while the low-salt diet was being given, the plasma norepinephrine level while the high-salt diet was being given, and the percentage of body weight made up by fat. Fifty-one of the obese adolescents were also studied before and after a 20-week weight-loss program. After the weight-loss program, the 36 subjects who lost more than 1 kg of body weight had a reduced sensitivity of blood pressure to sodium (difference from value during high-salt diet to that during low-salt diet, -1 +/- 1 mm Hg). The blood pressure of the remaining 15 adolescents was still sensitive to sodium intake (-11 +/- 3 mm Hg). These results support the hypothesis that the blood pressure of obese adolescents is sensitive to dietary sodium intake and that this sensitivity may be due to the combined effects of the hyperinsulinemia, hyperaldosteronism, and increased activity of the sympathetic nervous system that are characteristic of obesity.
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                Author and article information

                Journal
                Title: Hypertension
                Abbreviated Title: Hypertension
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 0194-911X
                ISSN (Electronic): 1524-4563
                Publication date Created: March 1996
                Publication date (Print): March 1996
                Volume: 27
                Issue: 3
                Pages: 481-490
                Affiliations
                [1 ]From Indiana University School of Medicine, Indianapolis.
                Article
                DOI: 10.1161/01.HYP.27.3.481
                PubMed ID: 8613190
                SO-VID: 8d76c6a5-2d39-4818-a586-e874a5bd64e0
                Copyright © © 1996
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